Biomedical subjects

S M Friedman

Publications and source records attributed to S M Friedman.

204 records · Page 12Linked to original sources

PubMedDate not supplied

Evidence for enhanced sodium transport in the tail artery of the spontaneously hypertensive rat.

Transmembrane Na+ and K+ gradients in the rat tail artery were dissipated by overnight incubation in K-free PSS at 10 degrees C and then allowed to recover in normal physiologic salt solution (PSS) at 37 degrees C. The active extrusion of Na+ and uptake of K+ during the recovery period was monitored with Na+ and K+ selective glass electrodes. Passive exchanges were differentiated by re-admitting K+ at 3 degrees C, or in the presence of 1 mM ouabain at both 3 degrees C and 37 degrees C. Active exchange was switched on by an abrupt transfer of the tissue from 3 degrees C to 37 degrees C. Active exchange, measured in perfused, superfused, or sequentially incubated arteries, was distinctly enhanced in young (16-, 20- and 26-week-old) spontaneously hypertensive rats (SHR) of the Okamoto strain compared with age-matched Wistar-Kyoto normotensive (WKY) controls. No such difference was observed in rats with hypertension of 7 or 12 weeks' duration and equal severity induced by unilateral constriction of the renal artery. Steady-state Nai and Ki were measured after washing the tissues for 45 minutes at 3 degrees C in lithium-substituted medium to exchange extracellular sodium with lithium. Cell sodium in these tissues was further partitioned into a free component proportional to [Na]0 and an independent, constrained component. Cell potassium was found to be distinctly elevated in 2- and 4-month-old SHR, while free cell sodium remained normal, despite increased cell permeability demonstrable in a significant exchange of lithium for cell potassium and sodium even at 3 degrees C.

Animals↗

PubMedDate not supplied

Evidence for an enhanced transmembrane sodium (Na+) gradient induced by aldosterone in the incubated rat tail artery.

Aldosterone is known to stimulate Na+ transport as measured in terms of current-carrying capacity of epithelial sheets or of Na+ - K+ ATPase activity in cells. The possibility that this is reflected in an altered steady-state transmembrane Na+ distribution in vascular smooth muscle was here examined directly. Transmembrane Na+ and K+ gradients were first dissipated by overnight incubation in K-free physiological salt solution (PSS) at 10 degrees C and then reestablished by 3 hours in normal PSS at 37 degrees C. The addition of d-aldosterone (but not corticosterone) to these media significantly reduced cell Na. This involved only free cell Na which was reduced by about 20% of 3 mmole/kg dry wt. No significant change in membrane permeability measured in terms of net Li uptake at 3 degrees C or at 37 degrees C was observed. The lowest effective aldosterone concentration was 2.8 x 10(-9) M. These results are consistent with the observed enhancement of net Na+ transport in incubated arteries in DOCA-induced hypertension and in the SHR but do not account for the increased Na+ permeability observed in these states.

Aldosterone↗

PubMedDate not supplied

Direct measurement of sodium influx in vascular smooth muscle. Stimulation by aldosterone.

The influx of 22Na into the smooth muscle cells of incubated rat tail arteries was measured directly, in the presence and absence of 2.8 X 10(-7) M D-aldosterone. During the analysis, extracellular 22Na and 23Na were removed by incubation of the tissue in sodium-free lithium-substituted physiological salt solution at less than 3 degrees C. Aldosterone increased the influx rate coefficient by 10% (0.104 +/- 0.004 [SE] min-1, n = 13, vs 0.095 +/- 0.003 [SE] min-1, n = 13 without aldosterone; p less than 0.01) but did not significantly reduce the sodium content. We conclude from direct measurements that aldosterone acts to increase the influx of sodium in incubated tail arteries from normal rats; we conclude from measurements of the sodium influx and sodium content that aldosterone also acts to increase the efflux of sodium in this preparation.

Aldosterone↗

PubMedDate not supplied

Optic nerve avulsion secondary to a basketball injury.

Optic nerve avulsion secondary to a basketball injury is a rare complication. The patient underwent a vitrectomy for a non-clearing vitreous hemorrhage. The nerve was partially avulsed with multiple choroidal ruptures in the fovea. It was concluded that optic nerve disorders rarely occur after basketball injuries. Patients with a dense vitreous hemorrhage may benefit from a vitrectomy although the vision will be limited by the optic nerve disorder.

Adolescent↗

PubMedDate not supplied

[Triggering of human peripheral blood B cells by supernatants of activated T cells: the role of Ia-like determinants].

Human peripheral blood B lymphocytes, isolated by Sephadex G-200 anti-Fab column chromatography, were non specifically induced by either pokeweed mitogen (PWM) or soluble products of antigen stimulated T cells, to differenciate into plaque directed against human Ia-like antigens (anti-p 23-30) inhibited the differenciation of B cells into antibody forming cells. Thus, while PWM induced proliferation was only mildly reduced by anti-p 23-30, the PWM induced PFC response was totally abrogated. Conversely, the antiserum abolished both the proliferative and the PFC responses generated by products of activated T cells. Using both Ouchterlony plates and co-precipitation techniques, we were unable to detect p 23-30 molecules on the active products present in the T cells supernatants. These data suggest that the inhibitory effects are secondary to interaction of the antiserum with B cells determinants.

B-Lymphocytes↗

PubMedDate not supplied

Additive effects of aldosterone with vasopressin or angiotensin.

Rat tail arteries were incubated overnight in potassium (K)-free physiological saline solution (PSS) at 10 degrees C, then returned to normal aerated PSS at 37 degrees C for a 3-hour recovery period followed by standard chemical analysis. Cell sodium (Na) was measured following replacement of extracellular Na by lithium (Li) at 3 degrees C. The addition of aldosterone at 10(-7) M reduced free cell Na by about 3 mmol/kg dry weight (about 20%). Arginine vasopressin also lowered cell Na to the same degree. The minimal effective dose was about 25 pM (25 pg/ml, 0.01 mU/ml), and the maximal dose was about 250 pM. No effect was seen with higher doses (greater than 1.5 nM or 0.5 mU/ml). Tissues incubated in media containing 10(-7) M aldosterone showed an exaggerated response to vasopressin evidenced by a near doubling of the maximum fall in cell Na produced by a tenfold smaller dose (25 pM). No significant change in cell K was observed while cell water tended to increase with lower doses. Angiotensin produced a similar reduction of cell Na at the same dose levels as vasopressin and was similarly additive with aldosterone. We suggest that these hormones enhance the transport of Na from luminal to basal sides of polarized cells and from cells to environment in symmetrical cells.

Aldosterone↗